Lactate production and absence of gluconeogenesis from placental substrates in fetuses from fed and 48-H starved rats.

Abstract

Fed and 48-h starved rats were infused on day 21.5 of gestation for 20 min through the left uterine artery with (U-14C-]-o-glucose, (U-14C]-glycerol, or (U-14C] -L-alanine. The mother and fetuses from both uterine horns were processed separately for radioactivity measurements in plasma and liver. Differences in radioactivity values between fetuses from the left and the right sides are used as indexes of placental transference of the infused tracers prior to their distribution and transformation in the maternal circulation. After infusion of (U-14C]-o-glucose, (U-14C] -glycerol, or (U-14C]-L-alanine, plasma radioactivity values and specific activities corresponding to the respective infused tracer appeared much higher in fetuses from the left than the right uterine side. Plasma 14C-lactate values also were higher in the left than the right fetuses indicating that fetoplacental structures produced lactate from those placentally transferred 14C-metabolites. No difference in plasma 14C-glucose between left and right uterine horn fetuses was observed after maternal infusion with either [U-14C]-glycerol or [U-14C]-L-alanine, either in fed or 48-h starved rats. In the mother both [U-14C]-glycerol and [U14C]-L-alanine were efficiently converted to 14C-glucose, and this process was significantly enhanced with starvation. 14C-fatty acids present in fetal liver after maternal infusions with either (U-14C]-o-glucose or [U-14C]-glycerol were decreased by starvation whereas no fatty acid synthesis from (U-14C]-L-alanine was detected. Much less 14C-glyceride glycerol was found in fetal liver after maternal infusions of (U-14C]-o-glucose than (U-14C]-glycerol, and its incorporation was unaffected by maternal starvation. Results show the significant production by the fetoplacental unit of lactate from transferred maternal substrates and the absence of gluconeogenesis in the rat fetus even after 48 h of maternal food deprivation. Lack of gluconeogenesis occurred even above the triose phosphate step and despite the fact that glycerol phosphorylation is active in fetal liver, indicating that maternal glucose is the only source of this metabolite for the normal rat fetus.